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Influence of a monocyte chemoattractant protein 1 mutated allele on the response to protease inhibitor‐based antiretroviral therapy
Author(s) -
Coll B,
AlonsoVillaverde C,
Parra S,
Rabassa A,
Martorell L,
Joven J,
Masana L
Publication year - 2006
Publication title -
hiv medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.53
H-Index - 79
eISSN - 1468-1293
pISSN - 1464-2662
DOI - 10.1111/j.1468-1293.2006.00392.x
Subject(s) - viral load , allele , medicine , immunology , chemokine , protease inhibitor (pharmacology) , genotype , monocyte , virology , chemokine receptor ccr5 , chemokine receptor , biology , virus , gene , inflammation , antiretroviral therapy , genetics
Background Antiretroviral drug efficacy has been widely studied in relation to viral factors. Mutations in the HIV co‐receptors and their natural chemokines, however, may be critical in HIV infection and treatment response. We compared the efficacy of protease inhibitor (PI) treatment among PI‐naïve patients grouped according to whether they carried the chemokine CC motif receptor 2 ( CCR‐2 ) 64I and monocyte chemoattractant protein 1 ( MCP‐1 )–2518G alleles. Methods and results HIV‐infected patients who were PI‐naive were selected for the study ( n =164) but there was no restriction on lymphocyte CD4 count or plasma HIV viral load. Follow‐up was for the first 24 months of treatment. Clinical and laboratory data were obtained every 3 months. All the participants were genotyped for the MCP‐1 –2518G, CCR‐2 64I, CCR‐5 Δ32 and stromal derived factor 1 ( SDF1 ) 3′A mutated alleles. The results indicated that patients carrying the mutated allele of MCP‐1 had a higher mean CD4 cell count throughout the follow‐up period than those with the common allele ( P= 0.01). Also, patients with the MCP‐1 and CCR‐2 mutated alleles were more likely to continue to have an undetectable viral load following treatment ( P= 0.05). Conclusion A better response to PI treatment appears to be conferred by mutations in the host MCP‐1 and CCR‐2 genes, and may be related to the cellular axis‐of‐entry used by the retrovirus.